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Polystyrene microplastics arrest skeletal growth in puberty through accelerating osteoblast senescence
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Researchers found that polystyrene microplastics accumulated in the bones of mice during puberty, leading to reduced body and bone length and impaired bone structure. The microplastics accelerated premature aging (senescence) of bone-building cells called osteoblasts, suppressing their ability to form new bone. The study suggests that microplastic exposure during critical growth periods may pose a risk to skeletal development.
Polystyrene microplastics (PS-MPs) have attracted worldwide attention to their massive accumulation in terrestrial and aquatic ecosystems. It has been demonstrated that MPs are easily to accumulate in organs and exert toxic effects. However, their exposure risk to the skeleton remains unknown. In this study, we observed PS-MPs accumulation in both the long bones and axial bones, leading to reduced body length, as well as femur and tibia length. PS-MPs treated mice exhibited redundant skeletal growth and impaired trabecular bone micro-architecture, which is due to the suppressed osteogenic ability as the number of osteoblasts decreased significantly in PS-MPs treated mice. In histological analysis, we observed the accumulation of senescent osteoblasts in the bone trabecula of PS-MPs treated mice, as well as the impaired autophagy with decreased autophagosome and reduced autophagy-related proteins in the senescent osteoblasts. Re-establishing autophagy effectively reversed the senescent phenotype in osteoblasts and ameliorated PS-MPs induced skeletal growth arrest. Hence, our study reveals the detrimental role of PS-MPs in skeletal growth in puberty through accelerating osteoblast senescence, which may be alleviated by reactivating the autophagy. This study provides new evidence of the PS-MPs on health threats and the potential therapeutic targets to reverse it.
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Polystyrene microplastics induces senescence of osteocytes by activating the cyclooxygenase-2 signaling pathway
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Researchers found that polystyrene microplastics can be taken up by osteocytes, the most abundant cells in bone tissue, and cause them to undergo premature aging through a process called senescence. The microplastics triggered oxidative stress and activated a specific inflammatory signaling pathway involving cyclooxygenase-2. The study suggests that microplastic exposure could potentially impair bone health by disrupting the normal function of the cells responsible for maintaining bone tissue.
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Mice that drank water containing polystyrene microplastics for six months developed significant bone loss resembling osteoporosis, with weakened bone structure and reduced bone formation. The microplastics triggered inflammation in bone stem cells and disrupted the balance between bone-building and bone-breaking processes, suggesting that long-term microplastic exposure could contribute to bone disease.
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Rats given high doses of polystyrene microplastics for four weeks showed bone loss, weaker bone-forming cells, and disrupted bone-resorbing cells, along with changes in metabolism and inflammation-linked aging processes. Lower doses caused minimal effects. Researchers identified two chemical changes that could serve as early markers of microplastic-related bone damage.
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Researchers exposed human bone-building cells (osteoblast-like cells) to polystyrene microplastics in a lab setting. The cells showed reduced signals linked to building new bone and increased signals linked to bone breakdown, suggesting microplastics may affect cell activity related to bone health.
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